Cancer Center, Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Genes Dev. 2012 Apr 15;26(8):751-5. doi: 10.1101/gad.191163.112.
In the April 1, 2012, issue of Genes & Development, Simon and colleagues (pp. 651-656) demonstrated that the disruption of Ezh2 in mice is sufficient to cause T-acute lymphoblastic leukemia (T-ALL). Moreover, in concert with concurrent studies, the authors revealed that similar mechanisms are involved in human T-ALL. These data contrast with previous findings showing that increased EZH2 activity promotes cancer.
在 2012 年 4 月 1 日的《基因与发育》杂志上,Simon 及其同事(第 651-656 页)证明,破坏小鼠中的 Ezh2 足以导致 T 急性淋巴细胞白血病(T-ALL)。此外,与同期研究结果一致,作者揭示了类似的机制也涉及人类 T-ALL。这些数据与先前的发现形成对比,先前的发现表明增加 EZH2 活性会促进癌症。